SULT1A1 genotype, active and passive smoking, and breast cancer risk by age 50 years in a German case–control study

Breast Cancer Research

Jenny Chang-Claude¹  Silke Kropp¹  Angela Risch²  Carmen Lilla¹ 

[1] Division of Clinical Epidemiology, German Cancer Research Center, Heidelberg, Germany;Division of Toxicology and Cancer Risk Factors, German Cancer Research Center, Heidelberg, Germany

关键词: sulfotransferase;    smoking;    polymorphism;    breast cancer;   

Others  :  1114992
DOI  :  10.1186/bcr976

 received in 2004-08-11, accepted in 2004-11-25,  发布年份 2005

【 摘 要 】

Introduction

Sulfotransferase 1A1 (encoded by SULT1A1) is involved in the metabolism of procarcinogens such as heterocyclic amines and polycyclic aromatic hydrocarbons, both of which are present in tobacco smoke. We recently reported a differential effect of N-acetyltransferase (NAT) 2 genotype on the association between active and passive smoking and breast cancer. Additional investigation of a common SULT1A1 genetic polymorphism associated with reduced enzyme activity and stability might therefore provide deeper insight into the modification of breast cancer susceptibility.

Methods

We conducted a population-based case–control study in Germany. A total of 419 patients who had developed breast cancer by age 50 years and 884 age-matched control individuals, for whom risk factor information and detailed smoking history were available, were included in the analysis. Genotyping was performed using a fluorescence-based melting curve analysis method. Multivariate logistic regression analysis was used to estimate breast cancer risk associated with the SULT1A1 Arg²¹³His polymorphism alone and in combination with NAT2 genotype in relation to smoking.

Results

The overall risk for breast cancer in women who were carriers of at least one SULT1A1*2 allele was not significantly different from that for women with the SULT1A1*1/*1 genotype (adjusted odds ratio 0.83, 95% confidence interval 0.66–1.06). Risk for breast cancer with respect to several smoking variables did not differ substantially between carriers of the *2 allele and noncarriers. However, among NAT2 fast acetylators, the odds ratio associated with passive smoking only (3.23, 95% confidence interval 1.05–9.92) was elevated in homozygous carriers of the SULT1A1*1 allele but not in carriers of the SULT1A1*2 allele (odds ratio 1.28, 95% confidence interval 0.50–3.31).

Conclusion

We found no evidence that the SULT1A1 genotype in itself modifies breast cancer risk associated with smoking in women up to age 50 years. In combination with NAT2 fast acetylator status, however, the SULT1A1*1/*1 genotype might increase breast cancer risk in women exposed to tobacco smoke.

【 授权许可】

   
2005 Lilla et al., licensee BioMed Central Ltd.

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